Evidence map›Paper›PMID 32216830›Full record

ArticleArthritis research & therapy2020

Resolvin D1 suppresses pannus formation via decreasing connective tissue growth factor caused by upregulation of miRNA-146a-5p in rheumatoid arthritis.

Weiwei Sun, Jinglan Ma, Han Zhao, Chipeng Xiao, Hao Zhong, Hanzhi Ling, Zhen Xie, Qingqing Tian, Huaijun Chen, Tingting Zhang and 3 more

Open access · goldAbstract read
In one paragraph

Article in Arthritis research & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
4.8field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

49 citing papers in PubMed, 81 citations in OpenAlex.

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  18. The oral microbiome in autoimmune diseases: friend or foe?Journal of translational medicine · 2023
    Review
  19. Article
  20. Targeting Angiogenesis via Resolution of Inflammation.Cold Spring Harbor perspectives in medicine · 2023
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 1 institution in 1 country.

Weiwei SunDepartment of Biochemistry, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang Province, China.
Jinglan MaDepartment of Biochemistry, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang Province, China.
Han ZhaoDepartment of Biochemistry, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang Province, China.
Chipeng XiaoDepartment of Biochemistry, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang Province, China.
Hao ZhongDepartment of Biochemistry, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang Province, China.
Hanzhi LingDepartment of Biochemistry, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang Province, China.
Zhen XieDepartment of Biochemistry, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang Province, China.
Qingqing TianDepartment of Biochemistry, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang Province, China.
Huaijun ChenDepartment of Biochemistry, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang Province, China.
Tingting ZhangDepartment of Biochemistry, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang Province, China.
Mu ChenDepartment of Biochemistry, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang Province, China.
Shengwei JinDepartment of Anesthesia and Critical Care, the Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325027, Zhejiang Province, China. jinshengwei69@163.com.
Jianguang WangDepartment of Biochemistry, School of Basic Medical Sciences, Wenzhou Medical University, Wenzhou, Zhejiang Province, China. wz_wjg@163.com.
Wenzhou Medical University · CN

Funding

Key Research and Development Program of Zhejiang Province 2019C03023National Natural Science Foundation of China 81472055National Natural Science Foundation of China 81672129Natural Science Foundation of Zhejiang Province LQ17H190005Public Technology Applied Research Foundation of Zhejiang Province of China LGF18H060009the Administration of Zhejiang Traditional Chinese Medicine 2016ZA136Zhejiang College Students Innovative Entrepreneurial Training Program 2018R413011
6 · The paper itself

Abstract

backgroundRheumatoid arthritis (RA) is a chronic autoimmune disease characterized by inflammation and joint stiffness, finally leading to tissue destruction. Connective tissue growth factor (CTGF) is a critical factor in RA progression, which promotes fibroblast-like synoviocyte (FLS) proliferation, pannus formation, and the damage of cartilage as well as bone. Resolvin D1 (RvD1) can promote inflammation resolution in acute inflammatory diseases, and recently, effects of RvD1 on chronic inflammatory diseases also attracted attention. This study aimed to examine the effect of RvD1 on pannus formation in RA and the underlying mechanism.

methodsSerum levels of RvD1 and CTGF were determined in RA patients and healthy persons by UPLC-MS/MS and ELISA respectively. The levels of CTGF and inflammatory factors were assessed by qRT-PCR and ELISA. MicroRNA expression profile was determined by miRNA microarray. The effects of CTGF, RvD1, and miR-146a-5p on angiogenesis were evaluated with tube formation and chick chorioallantoic membrane (CAM) assays. Collagen-induced arthritis (CIA) mice were constructed to detect the effects of RvD1 and miR146a-5p on RA. STAT3 activation was determined by Western blotting.

resultsRvD1 levels decreased while CTGF levels increased in RA patients' serum, and an inverse correlation of the concentrations of RvD1 and CTGF in the serum of RA patients was synchronously observed. In CIA mice, RvD1 suppressed angiopoiesis and decreased the expression of CTGF. Simultaneously, RvD1 significantly decreased CTGF and pro-inflammation cytokines levels in RA FLS. Furthermore, CTGF suppressed angiopoiesis and RvD1 inhibited the proliferation and migration of RA FLS and angiopoiesis. MiRNA microarray and qRT-PCR results showed that RvD1 upregulated miRNA-146a-5p. The transfection experiments demonstrated that miRNA-146a-5p could decrease inflammatory factors and CTGF levels. Moreover, miRNA-146a-5p decreased the proliferation of FLS and angiogenesis in vivo. MiRNA-146a-5p also suppressed angiogenesis and downregulated the expression of CTGF in CIA mice. Finally, Western blot results revealed that miRNA-146a-5p inhibited the activation of STAT3.

conclusionRvD1 is prone to alleviate RA progression through the upregulation of miRNA-146a-5p to suppress the expression of CTGF and inflammatory mediators, thereby decreasing pannus formation and cartilage damage.

Indexed as

AnimalsArthritis, ExperimentalArthritis, RheumatoidCells, CulturedConnective Tissue Growth FactorCytokinesDocosahexaenoic AcidsFemaleFibroblastsGene ExpressionHumansMaleMice, Inbred DBAMicroRNAsMiddle AgedPannusConnective Tissue Growth FactorCytokinesDocosahexaenoic AcidsMicroRNAsresolvin D1Connective tissue growth factorInflammatory mediatorsMiRNA-146a-5pPannusResolvin D1Rheumatoid arthritis

Identifiers

PMID32216830
PMCPMC7099804
OpenAlexW3013578603

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.